Prostate cancer is a molecularly heterogeneous disease with recently characterized cancer-specific gene aberrations (Lapointe J. et al., Cancer Research 67:8504-8510 (2007); Demichelis F. et al., Genes Chromosomes Cancer 48:366-380 (2009); Berger M F et al., Nature 470:214-220 (2011)). The most common genetic alteration found in prostate cancer is TMPRSS2-ERG gene fusion, which occurs in approximately 50% of cases (Kumar-Sinha C. et al., Nat Rev Cancer 8:497-511 (2008); Mosquera J M et al., Clin Cancer Res 15:4706-4711 (2009); Tomlins S A et al., Eur Urol 56:275-286 (2009); Tomlins S A et al., Science 310:644-648 (2005)). ERG over-expression due to the androgen-regulated TMPRSS2 gene is a proxy for the gene fusion and serves as a prostate cancer-specific biomarker (Park K. et al., Neoplasia 12:590-598 (2010)). The detection of over-expressed cancer-associated genes from expression profiling analyses has introduced novel potential biomarkers (Tomlins S A et al., Cancer Cell 13:519-528 (2008); Luo J. et al., Cancer Res 61:4683-4688 (2001); Qian D Z et al., Clin Cancer Res 15:3135-3142 (2009); Magee J A et al., Cancer Res 61:5692-5696 (2001); Welsh J B et al., Cancer Res 61:5974-5978 (2001)). TFF3 is one of the three members of the TFF gene family located near TMPRSS2 on chromosome 21q22.3. Besides their prominent expression in mucous epithelia, these peptides are also synthesized in the central nervous system (Jagla W. et al., FASEB J 14:1126-1131 (2000)). It has been reported that TFF3, over-expressed in about 50% of prostate cancers and inhibited by concurrent ERG expression and AR signaling (Rickman D S et al., Neoplasia 12:1031-1040 (2010); Faith D A et al., Prostate 61:215-227 (2004); Garaway I P et al., Prostate 61:209-214 (2004)), is also involved in regulation of cell migration, invasion, and angiogenesis in other cancers.